Several different circumstances which increase the production of O2 minus within E. coli, also increase the rate of synthesis of the manganese superoxide dismutase. Since this was seen at constant pO2, the induction could not have been due to O2, but could have been due to O2-or to some product uniquely derived therefrom. We will attempt to demonstrate this induction in broken cell preparations, where permeability barriers do not exist. The length of the lag between application of O2- and the initiation of induction may allow us to distinguish between these possibilities. We will also be able to search for a gratuitous inducer by testing compounds thought likely to bind to the repressor, in competition with O2-. We will extend studies of the mechanism of induction to yeast. We will further explore the physiological roles of the superoxide dismutases through the isolation and characterization of mutants with defects in these enzymes. The mutagenicity of O2- and the possibility that it can give rise to singlet oxygen will also be explored.